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The mechanism of enhancement/inhibition of quartz toxicity induced by iron is still unclear. Here the amount of iron on a fibrogenic quartz (Qz) was increased by wet impregnation (Fe(NO3)30.67 and 6.7 wt %). X-ray diffraction (XRD), XRF diffuse reflectance, UV−vis, and infrared (IR) spectroscopies revealed dispersed ferric ions, and hematite aggregates at the higher loading. Surface features relevant to pathogenicity and cell responses were compared not only to the original quartz but also to reference quartz DQ12. Surface charge (ζ-potential) was more negative on the original and low-loaded specimen than on the high-loaded one. DQ12 had a less negative ζ-potential than Qz, ascribed to the absence of aluminium present in Qz (1.7 wt %). All quartz specimens were able to generate HO•radicals, iron-loaded samples being more reactive than original quartz. Iron deposition inhibited the rupture of a C−H bond. All quartzes were phagocytized by alveolar macrophages (AMΦ cell line NR8383) to the same extent, irrespective of their surface state. Conversely, iron loading increased AMΦ viability (evaluated by cytotoxicity and induction of apoptosis). Qz was found to be much less cytotoxic than DQ12. The induction of oxidative stress and inflammatory responses (evaluated by HO-1 mRNA expression and TNF-α mRNA and protein expression) revealed a reduction in inflammogenicity upon iron loading and a more inflammogenic potency of DQ12 ascribed to undissociated SiOH interacting via H-bonding with cell membrane components. The results suggest that besides aluminium also iron at the quartz surface may have an inhibitory effect on adverse health responses. [ABSTRACT FROM AUTHOR]

To understand the effect of the commercial processing of diatomaceous earths (DEs) on their ultimate surface structure and potential toxicity, we investigated the influence of the industrial processing and the nature of the deposit. Two flux calcined specimens from different deposits, DE/1-FC and DE/2-FC, and the simply calcined sample DE/1-C, from the same deposit as DE/1-FC, were compared in both their bulk and their surface properties. X-ray diffraction (XRD) analysis in a heating chamber revealed the presence of cristobalite in all samples, more abundant on the flux calcined ones. The crystal lattice is probably imperfect, as the α−β transition, visible by XRD in DE/1-FC and DE/2-FC, is not detected by differential scanning calorimetry. Progressive etching with HF solutions suggests that most of the crystalline phase is at the core and not at the outer region of the samples. The combined use of spectroscopic (UV−vis and IR) and calorimetric techniques (heat of adsorption of water as a measure of hydrophilicity) reveals that DE/1-FC and DE/2-FC particles have an external layer of glass, absent in DE/1-C, where iron impurities act as network-forming and sodium ions as modifier species, with few patches of a hydrophobic phase, the latter relatable to a heated pure silica phase. When tested on a macrophage cell line (MH-S) in comparison with appropriate positive and negative controls (an active and an inactive quartz dust, respectively), only DE/1-C exhibited a cell damage and activation similar to that of active quartz (measured by lactate dehydrogenase release, peroxidation of membrane lipids and synthesis of NO). It is likely that the presence of a vitreous phase mitigates or even eliminates the cellular responses of silica in DE. [ABSTRACT FROM AUTHOR]

In order to evaluate the effect of thermal treatments on the surface reactivity and carcinogenic potential of diatomaceous earth (DE) products, the physicochemical features of some specimens—derived by heating the same original material—were compared with their cytotoxic and transforming potency. The samples were an untreated DE (amorphous) progressively heated in the laboratory at 900°C (DE 900) and 1200°C (DE 1200) and a commercial product manufactured from the same DE (Chd) from which the finer fraction (< 10–μm diameter) was separated (Chd-F). Quartz (Min-U-Sil 5) and a vitreous silica (amorphous) smoothed up with hydrofluoric acid and were used as positive and negative controls, respectively. All samples were analyzed for their degree of crystallization, for their ability to release free radicals and reactive oxygen species, and for their cytotoxic and transforming potencies in Syrian hamster embryo (SHE) cells. X-ray diffractometry showed that DE 900, like DE, was still amorphous, whereas DE 1200 as well as the commercial product (Chd) were partially crystallized into cristobalite. The ability of the dust to release hydroxyl (•OH) radicals in the presence of hydrogen peroxide, as revealed by the spin-trapping technique, was as follows: Chd-F, DE 1200 > Chd > DE 900 > DE, suggesting that on heating, the surface acquires a higher potential for free radical release. Most of the silica samples generated COO• radicals from the formate ion, following homolytic rupture of the carbon-hydrogen bond, in the presence of ascorbic acid. A concentration-dependent decrease in cell proliferation and colony-forming efficiency was observed in SHE cultures treated with Chd-F, Chd, and DE. Heating abolished DE cytotoxicity but conferred a transforming ability to thermal treated particles. DE was the only sample that did not induce morphological transformation of cells. According to their transformation capacity, the samples were classified as follows: Chd-F > Chd, DE 1200 > DE 900 ≫ DE. Taken together, the reported results suggest that (1) the transforming potential of a biogenic amorphous silica is related to the thermal treatment that transforms the original structure in cristobalite and generates surface active sites; (2) the reactivity of samples in releasing •OH radicals correlates to their transforming ability; (3) the finer fraction of the commercial product is significantly more toxic and transforming than the coarse dust; and (4) opposite to silica dusts of mineral origin, which loose both cytotoxicity and transforming ability upon heating, heated diatomite acquires a cell-transforming potency. DE products should be thus considered a set apart of silica-based potentially toxic materials. [ABSTRACT FROM AUTHOR]

Four commercial quartz dusts (flours), two inflammogenic in vivo and activating macrophages in vitro (Qz 2/1-c and Qz 3/1-c) and two mostly inert (Qz 5/1-c and Qz 11/1-c), have been compared regarding their surface properties, in order to detect chemical differences which may account for their different biological behaviour. The following features have been examined: 1) extent of the amorphous fraction (heat associated α↔β transition of quartz) and its solubility in HF; 2) potential to cleave a carbon-hydrogen bond with consequent generation of carbon centred radicals (spin trapping technique, EPR); 3) evolution of surface functionalities upon heating (FTIR spectroscopy); 4) mechanisms of adsorption of water on dusts outgassed at 150° and at 800 °C (adsorption calorimetry). HCl treated samples have also been examined. The two "less toxic" quartzes are more resistant to HF attack, coordinate irreversibly H2O molecules and exhibit strong adsorption sites, which are absent in the other two and in a very pure quartz dust. Conversely all samples show the same potential to release free radicals. The different behaviour of the two sets of dust is consistent with a different level of impurities, namely aluminium ex kaolin, carbon and alkaline ions. The less inflammogenic quartzes appear to be covered by aluminium ions (and possibly iron) which strongly holds molecular water or carbonates, thus reducing the silanol patches to a large extent and changing the surface properties of the particles. We hypothesize that cellular response, and particularly macrophage activation and death, is mediated by strong interactions between silanol patches and some cell membrane components, but inhibited when the surface of the particle is modified by the presence of aluminium ions, surface carbonates and other metal contaminants. This hypothesis suggests that grinding procedures with little appropriate additives, e.g. kaolin, alumina, can reduce the biological activity of quartz dusts. [ABSTRACT FROM AUTHOR]